To assess the importance of B cell control of T cell differentiation,
we analyzed the course of the T helper type 1 (T(H)1)-driven disease experimental
autoimmune encephalomyelitis in mice with an altered B cell compartment.

We found that recovery was dependent on the presence of autoantigen-reactive
B cells.

B cells from recovered mice produced interleukin 10 (IL-10) in
response to autoantigen.

With a bone marrow chimeric system, we generated
mice in which IL-10 deficiency was restricted to B cells but not T cells.

In the absence of IL-10 production by B cells, the pro-inflammatory type
1 immune response persisted and mice did not recover.

These data show that
B cell#150;derived IL-10 plays a key role in controlling autoimmunity.